The Journal of Experimental Medicine
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Published 20 June 2005. doi:10.1084/jem.20050112
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 201, Number 12, 1905-1913
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ARTICLE

 A chromosomally integrated bacteriophage in invasive meningococci

Emmanuelle Bille1, Jean-Ralph Zahar1, Agnes Perrin1, Sandrine Morelle1, Paula Kriz2, Keith A. Jolley3, Martin C.J. Maiden3, Catherine Dervin4, Xavier Nassif1, and Colin R. Tinsley1,4

1 Institut National de la Santé et de la Recherche Medicale U570, Faculté de Médecine Necker, 75015 Paris, France
2 National Reference Laboratory for Meningococcal Infections, National Institute of Public Health, 100 42 Prague, Czech Republic
3 The Peter Medawar Building for Pathogen Research and Department of Zoology, Oxford, OX1 3SY, England, UK
4 Institut National Agronomique Paris-Grignon, 75231 Paris, Cedex 05, France

CORRESPONDENCE Xavier Nassif: nassif{at}necker.fr

Cerebrospinal meningitis is a feared disease that can cause the death of a previously healthy individual within hours. Paradoxically, the causative agent, Neisseria meningitidis, is a common inhabitant of the human nasopharynx, and as such, may be considered a normal, commensal organism. Only in a small proportion of colonized people do the bacteria invade the bloodstream, from where they can cross the blood–brain barrier to cause meningitis. Furthermore, most meningococcal disease is caused by bacteria belonging to only a few of the phylogenetic groups among the large number that constitute the population structure of this genetically variable organism. However, the genetic basis for the differences in pathogenic potential remains elusive. By performing whole genome comparisons of a large collection of meningococcal isolates of defined pathogenic potential we brought to light a meningococcal prophage present in disease-causing bacteria. The phage, of the filamentous family, excises from the chromosome and is secreted from the bacteria via the type IV pilin secretin. Therefore, this element, by spreading among the population, may promote the development of new epidemic clones of N. meningitidis that are capable of breaking the normal commensal relationship with humans and causing invasive disease.

Abbreviations used: MDA, meningococcal disease associated; ORF, open reading frame; ST, sequence type.

E. Bille and J.-R. Zahar contributed equally to this work.


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